We have demonstrated i experimental animals that the local and distant organ injury from a period of artery blockage and subsequent re- establishment of blood flow is severe, and that it is attenuated by clocking one portion of the host's inflammatory system; the complement system. This means that tissue which was not otherwise to be lost on the basis of the arterial occlusion alone was subsequently irreversibly damaged by the host inflammatory response. Therapeutic blockage of such a response has the capacity to lessen injury, with a consequent diminution of mortality and disability. In further experiments in tissue culture, we have found, to our surprise, that the activation of the complement system depended on antibodies binding to the tissue, an event conventionally thought of as limited to auto-immune diseases. Since such a mechanism could be specifically treated with a crippled (or "F(ab')2") antibody, our aim is to precisely define the antigens to which these self-antibodies bind and the mechanism by which they appear. Our related goal is to prove therapeutic efficacy of such crippled antibodies or to improve the therapeutic potential of complement system inhibition.